How should developing countries manage diabetes?
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Alka Kanaya
Publications and source records attributed to Alka Kanaya.
Impact of inflammation on the relationship among alcohol consumption, mortality, and cardiac events: the health, aging, and body composition study.
BACKGROUND: Uncertainty remains about the overall survival benefit of alcohol consumption and the mechanisms underlying the cardioprotective effect of light to moderate alcohol intake. Recent evidence suggests an anti-inflammatory effect of light to moderate alcohol consumption. We investigated the relationship of alcohol intake with all-cause mortality and cardiac events and evaluated whether this relationship is mediated or modified by inflammatory markers. METHODS: The analysis included 2487 subjects, aged 70 to 79 years, without baseline coronary heart disease (CHD) or heart failure (HF), participating in the Health, Aging, and Body Composition study. All-cause mortality and incident cardiac events (CHD and HF) were detected during a mean follow-up of 5.6 years. Alcohol consumption and serum levels of interleukin-6 (IL-6) and C-reactive protein (CRP) were assessed at baseline. RESULTS: A total of 397 participants died, and 383 experienced an incident cardiac event. Compared with never or occasional drinkers, subjects drinking 1 to 7 drinks per week had lower age-, sex-, and race-adjusted incidences of death (27.4 vs 20.1 per 1000 person-years, respectively) and cardiac events (28.9 vs 20.8 per 1000 person-years). After adjustment for confounders, compared with never or occasional drinkers, light to moderate drinkers (1-7 drinks per week) showed a decreased risk of death (hazard ratio [HR], 0.75; 95% confidence interval [CI], 0.56-1.00) and cardiac events (HR, 0.72; CI, 0.54-0.97). Adjustment for potential mediators, and particularly inflammatory marker levels, did not affect the strength of this association. CONCLUSION: Light to moderate alcohol consumption was associated with significantly lower rates of cardiac events and longer survival, independent of its anti-inflammatory effect.
Aged↗
Preinfection systemic inflammatory markers and risk of hospitalization due to pneumonia.
RATIONALE: Elevated proinflammatory cytokines are associated with severity of pneumonia, but the role of preinfection cytokine levels in the predisposition to pneumonia in humans is less clear. OBJECTIVE: To ascertain role of preinfection inflammatory markers on susceptibility to community-acquired pneumonia (CAP). METHODS: Longitudinal analysis over 6.5 yr of a cohort that consisted of 70- to 79-yr-old well-functioning elderly individuals. MEASUREMENTS: Association between preinfection tumor necrosis factor (TNF), interleukin 6 (IL-6), and C-reactive protein (CRP) levels and CAP requiring hospitalization. RESULTS: Of the 3,075 participants, 161 (5.2%) developed at least one episode of CAP requiring hospitalization over a median duration of 3.3 yr. The highest tertiles of TNF (> 3.7 pg/ml) and IL-6 (> 2.4 pg/ml) were associated with increased risk of CAP, and the adjusted odds ratios were 1.6 (95% confidence interval [CI], 1.02-2.7) and 1.7 (95% CI, 1.1-2.8), respectively. The adjusted risk of CAP with at least one of these markers in the highest tertile was 1.6 (95% CI, 1.1-2.3). TNF and IL-6 levels in the highest tertile had a synergistic effect (p = 0.01 for interaction), and risk of CAP for both markers in the highest tertile was 2.8 (95% CI, 1.8-4.3). An FEV(1) of 50% or less of predicted was associated with the highest risk of CAP (adjusted odds ratio, 3.6; 95% CI, 2.3-5.6). Furthermore, TNF and IL-6 levels modified risk of CAP in participants with coexisting medical conditions and history of smoking. CONCLUSION: In the well-functioning elderly subjects, preinfection systemic levels of TNF and IL-6 were associated with higher risk of CAP requiring hospitalization in smokers and those with coexisting medical conditions.
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Association of metabolic syndrome with exercise capacity and heart rate recovery in patients with coronary heart disease in the heart and soul study.
It is not known whether the metabolic syndrome is associated with poor exercise capacity among patients who have established coronary heart disease. We evaluated the association of the metabolic syndrome with treadmill exercise capacity and heart rate recovery among patients who had coronary heart disease. We measured treadmill exercise capacity (METs) and heart rate recovery (beats per minute) in 943 subjects who had known coronary heart disease. Of these, 377 (40%) had the metabolic syndrome as defined by criteria of the National Cholesterol Education Program. Participants who had the metabolic syndrome were more likely to have poor exercise capacity (METs <5, 33% vs 18%, p <0.0001) and poor heart rate recovery (<or=16 beats/min, 34% vs 21%, p <0.0001) than those who did not have the metabolic syndrome. In ordinal logistic regression analyses, the metabolic syndrome was associated with decreased exercise capacity (odds ratio [OR] 2.2, 95% confidence interval [CI] 1.7 to 2.8, p <0.0001) and decreased heart rate recovery (OR 1.8, 95% CI 1.4 to 2.3, p <0.0001). These associations remained strong after adjusting for potential confounding variables (OR 1.6, 95% CI 1.2 to 2.1, p = 0.003 for decreased exercise capacity; OR 1.4, 95% CI 1.1 to 1.9, p = 0.02 for decreased heart rate recovery). The metabolic syndrome is independently associated with poor exercise capacity and poor heart rate recovery in patients who have established coronary heart disease. Decreased exercise capacity may contribute to the adverse outcomes associated with the metabolic syndrome.
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The metabolic syndrome, inflammation, and risk of cognitive decline.
CONTEXT: Several studies have reported an association between the metabolic syndrome and cardiovascular disease. Despite an increasing awareness that cardiovascular risk factors increase risk of cognitive decline and dementia, there are few data on the metabolic syndrome and cognition. OBJECTIVE: To determine if the metabolic syndrome is a risk factor for cognitive decline and if this association is modified by inflammation. DESIGN AND SETTING: A 5-year prospective observational study conducted from 1997 to 2002 at community clinics at 2 sites. PARTICIPANTS: A total of 2632 black and white elders (mean age, 74 years). MAIN OUTCOME MEASURES: Association of the metabolic syndrome (measured using National Cholesterol Education Program guidelines) and high inflammation (defined as above median serum level of interleukin 6 and C-reactive protein) with change in cognition (Modified Mini-Mental State Examination [3MS]) at 3 and 5 years. Cognitive impairment was defined as at least a 5-point decline. RESULTS: Compared with those without the metabolic syndrome (n = 1616), elders with the metabolic syndrome (n = 1016) were more likely to have cognitive impairment (26% vs 21%, multivariate adjusted relative risk [RR], 1.20; 95% confidence interval [CI], 1.02-1.41). There was a statistically significant interaction with inflammation and the metabolic syndrome (P = .03) on cognitive impairment. After stratifying for inflammation, those with the metabolic syndrome and high inflammation (n = 348) had an increased likelihood of cognitive impairment compared with those without the metabolic syndrome (multivariate adjusted RR, 1.66; 95% CI, 1.19-2.32). Those with the metabolic syndrome and low inflammation (n = 668) did not exhibit an increased likelihood of impairment (multivariate adjusted RR, 1.08; 95% CI, 0.89-1.30). Stratified multivariate random-effects models demonstrated that participants with the metabolic syndrome and high inflammation had greater 4-year decline on 3MS (P = .04) compared with those without the metabolic syndrome, whereas those with the metabolic syndrome and low inflammation did not (P = .44). CONCLUSION: These findings support the hypothesis that the metabolic syndrome contributes to cognitive impairment in elders, but primarily in those with high level of inflammation.
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Risk factors for mortality in middle-aged women.
BACKGROUND: Many factors contribute to mortality in older women, but their relative importance and independent contribution have been poorly characterized. METHODS: From 1990 to 1992, we assessed demographics, lifestyle measures, prevalent disease, medication use, anthropometrics, vital signs, and physical function in 17 748 postmenopausal women. We used proportional hazards modeling to evaluate their association with mortality. RESULTS: During 9 years of follow-up, 1886 women (10.6%) died. The relative hazard (RH) of death was approximately 1.5 (95% confidence interval [CI], 1.5-1.6) per 5 years of age, 1.4 (95% CI, 1.2-1.6) for a history of heart disease, and 1.9 (95% CI, 1.6-2.3) for a history of breast cancer. Modifiable risk factors associated with mortality included smoking (RH, 3.7 [95% CI, 3.1-4.5] for current smokers with a > or =50 pack-year history) and systolic blood pressure (RH, 1.3 [95% CI, 1.1-1.5], fifth vs first quintile). Elevated waist-hip ratio was associated with higher mortality (RH, 1.3 [95% CI, 1.1-1.5], fifth vs first quintile), but obesity was associated with lower mortality (RH, 0.7 [95% CI, 0.6-0.9] for body mass index [calculated as weight in kilograms divided by the square of height in meters] of >35.0 vs 18.5-25.0). Poor results on the timed Up and Go Test, a measure of physical function, were also strongly associated with mortality (RH, 1.7 [95% CI, 1.4-2.0], fifth vs first quintile). CONCLUSIONS: Simple measures are sufficient to stratify postmenopausal women into groups at high and low risk of dying. Smoking, central obesity, blood pressure, and physical function are potentially modifiable risk factors, although clinical trials are required to demonstrate that change in these factors affects mortality.
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